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The CRISPR system of the human pathogen Mycobacterium tuberculosis

  • Full or part time
    Prof M F White
  • Application Deadline
    Sunday, December 01, 2019
  • Competition Funded PhD Project (Students Worldwide)
    Competition Funded PhD Project (Students Worldwide)

Project Description

CRISPR is a prokaryotic adaptive immune system, allowing detection and degradation of invading viruses. For the public and much of the scientific community, CRISPR is now synonymous with the minimal Class 2 systems Cas9 and Cas12. However, many prokaryotes, including important pathogens such as Mycobacterium tuberculosis (Mtb), utilise a Type III CRISPR system that is complex, powerful and versatile to defend against attack. Type III systems synthesise a completely novel class of second messenger, cyclic oligoadenylate (cOA), when phage RNA is detected. cOA binds and activates a variety of downstream defence proteins. Our lab is at the forefront of research aimed at understanding and harnessing type III CRISPR systems and cOA signalling 1,2.

In this project, you will use a powerful combination of biochemistry, molecular biology and microbiology to study the type III CRISPR system of Mycobacterium tuberculosis (Mtb), building on recent advances in this area 3. The project will focus on the RNA targeting, cOA production and degradation by Mtb CRISPR and related enzymes, with the ultimate aim of developing this system into a tool for targeted RNA silencing in Mtb.

You will join a well-funded, experienced and friendly lab working on related aspects of CRISPR biology and DNA repair. Experience in microbiology and/or molecular biology would be advantageous, but training will be available. Please address informal enquires to Prof Malcolm White ( ).

Funding Notes

Eligibility requirements: Upper second-class degree or Masters in the broad area of Life Sciences.
Funding: Fees and stipend is provided for 3.5 years.

References

1 Rouillon, C., Athukoralage, J. S., Graham, S., Grüschow, S. & White, M. F. Control of cyclic oligoadenylate synthesis in a type III CRISPR system. eLife 7, e36734 (2018).
2 Athukoralage, J. S., Rouillon, C., Graham, S., Grüschow, S. & White, M. F. Ring nucleases deactivate Type III CRISPR ribonucleases by degrading cyclic oligoadenylate. Nature 562, 277-280, doi:https://doi.org/10.1101/380436 (2018).
3 Grüschow, S., Athukoralage, J. S., Graham, S., Hoogeboom, T. & White, M. F. Cyclic oligoadenylate signalling mediates Mycobacterium tuberculosis CRISPR defence. Nucl. Acids Res. 47, 9259-9270, doi:https://doi.org/10.1101/667758 (2019).

How good is research at University of St Andrews in Biological Sciences?

FTE Category A staff submitted: 50.45

Research output data provided by the Research Excellence Framework (REF)

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